Brady Pregerson, MD

: A 52-year-old female with a history of asthma presents to the emergency department for cough, tactile fever, and dyspnea. She denies syncope, palpitations, chest pain or other complaints. She states it feels like she is having an asthma attack but she hasn’t had one in over a decade so she did not have medicine for it at home.

: Vital signs are notable for a pulse of 134, blood pressure of 113/62, temperature 98.6, and sat of 95% on RA. Exam is notable for obesity, tachycardia and mild wheezing but good air movement and no respiratory distress. There is no leg edema.

Bronchitis, Asthma, Tachydysrhythmia, Pulmonary Embolism, Acute Coronary Syndrome.

EKG ANALYSIS, CASE OUTCOME & 1-MINUTE CONSULT:

(Peer reviewed by Dr. Stephen W. Smith of 

The computer read is correct: the rate is >100; there is a left axis; the voltage is <10mm in all limb leads (just barely); and, there are significant Q waves in two inferior leads (III & aVF), which could, among other possibilities, represent a prior completed inferior MI. There are other possible explanations for these Q-waves of course, including a normal variant or a pulmonary embolism (incomplete S1Q3T3 without the inverted T in III). There is also fairly significant tachycardia that is not explained by pain, albuterol use, fever or other conditions, so PE, again, could be the cause. Finally, there are nonspecific T-wave changes not called by the computer.

: The chest x-ray was clear with no cardiomegaly or infiltrate. Another important consideration for the differential diagnosis of low voltage and tachycardia is pericardial tamponade. A bedside echo showed no pericardial effusion (her low voltage was likely from obesity) but a possibly enlarged RV. The patient’s SOB did not improve with a trial of albuterol though her tachycardia actually ironically did improve. The WBC count was elevated at 17 with 22% bands and D-dimer was also elevated. Antibiotics were started and a chest CT was ordered to rule out PE and look for an x-ray negative pneumonia (~30% of cases of pneumonia only show up on CT, often done to check for PE). The CT showed no pneumonia but did show a saddle pulmonary embolism. The patient received half-dose tPA, was admitted and did well. No other cause of bandemia was found.



1. Consider PE with otherwise unexplained tachycardia. Though this EKG is quite nonspecific it is consistent with large PE. There will usually be other clinical findings but remember that 20% of PE’s are painless (typically the LARGE ones), and cough is present in ~1/4 of PE’s. While we are on the topic of PE and tachycardia, remember that you shouldn’t rule out PE just because there is no tachycardia as 75% of PE patients have a pulse <100 and 40% have a pulse <90.

2. Consider PE with an S wave in lead 1, especially when it is new and is in the proper clinical setting.

3. Consider PE with nonspecific T-wave changes, such as flattening, especially when they are new and are in the proper clinical setting.

4. Elevated WBC counts and even bandemia are not specific for infection.WBC is probably around 70% specific and band count around 90% specific. Any severe stress can cause demargination and elevated WBC count, not infrequently to levels >14 and occasionally to levels >30. If the cause of leukocytosis is not thought to be infectious, ordering a CRP and/or sed rate may be helpful as they will typically both be normal or if elevated only slightly so in the abscess of severe infection.

5. Conditions sometime mimic other conditions. In this case the patient felt like she was having an asthma attack, but that was unusual in that she hadn’t had one in over a decade.

Articles

The latest case report from Dr. Brady Pregerson concerns a 52-year-old female with a history of asthma presenting with a cough, tactile fever, and dyspnea. 

Case Report: Asthma or Something More?

: A 72-year-old male with a history of ESRD, CHF and DM presents to the hospital with 6 weeks of slowly progressive leg edema and 3 weeks of SOB/DOE that has become much worse over the past 24 hours and is associated with a new cough. He denies syncope, palpitations, chest pain, fever, or other complaints.

: Vital signs are normal except for a pulse-ox of 91% on room air and a RR of 30. Breath sounds are diminished but symmetric, and legs have symmetric pitting edema without erythema. His physical exam is otherwise normal.

 CHF, Pulmonary Embolism, Acute Coronary Syndrome, Pneumonia

T wave abnormality, consider inferolaeral ischemia

Do you agree with the computer? What should you do next?

EKG ANALYSIS, CASE OUTCOME, 1-MINUTE CONSULT & CASE LESSONS:

(peer reviewed by Dr. Stephen W. Smith of 

The computer read is correct but incomplete. There is ST elevation in aVR with semi-diffuse ST depression that is not caused by the RBBB. These EKG findings are concerning for subendocardial ischemia due to an incomplete coronary occlusion with insufficient flow to perfuse the entire myocardial wall. Since the subendocardium is more vulnerable to ischemia due to pressures within the myocardium, it can become ischemic even without complete occlusion. This causes ST depression in overlying leads with 

 ST elevation in aVR. In the proper clinical setting, this calls for urgent catheterization even though the occlusion is not complete because 1) there is ongoing ischemia and myocardial damage and 2) the partial occlusion can progress to complete occlusion if left untreated.

: Initial troponin was 8.0 (99% URL <0.030: troponin-i immunoassay, Abbott laboratories). Cardiology was consulted and the patient went to cath urgently. Repeat troponin a few hours after the first was 10.9. At cath, there was an 80% LAD occlusion that was stented.

ST elevation in aVR has many possible causes, one being reciprocal change to ST depression in left-sided leads as part of non-occlusive ACS causing subendocardial ischemia.

Always look for a reason when someone's condition has become worse in the past 24 hours. This patient initially seemed like routine CHF but his acute worsening was due to acute ischemia.

A 72-year-old male with a history of ESRD, CHF and DM presents to the hospital with 6 weeks of slowly progressive leg edema and 3 weeks of SOB/DOE that has become much worse over the past 24 hours and is associated with a new cough. What's your diagnosis?

Case Report: Congestive Heart Failure?

A 52-year-old female with a history of multiple sclerosis presents to the emergency department for generalized weakness and trouble swallowing that has gradually worsened over the past six days. She denies any syncope, palpitations, chest pain, dyspnea, fever, cough, sore throat or other complaints.

  Vital signs are normal except for a pulse of 115 beats per minute. Blood pressure is 140/88. Ear nose and throat exam is unremarkable and she is handling secretions without difficulty. The rest of her physical exam is otherwise non focal.

  Tachydysrhythmia, electrolyte abnormality, pulmonary embolism, acute coronary syndrome.

EKG read (see image on the right for initial EKG):

1. Sinus tachycardia
	2. Right atrial enlargement
	3. ST & T wave abnormality, consider inferior ischemia
	4. ST & T wave abnormality, consider anterolateral ischemia
	5. Abnormal ECG

Do you agree with the EKG read?  What should you do next?

(Peer reviewed by Dr. Stephen W. Smith of Dr. Smith’s ECG Blog)


	The computer read is correct. The ”right atrial enlargement” read is due to the large P-waves in leads II, III and aVF which is also known as P-pulmonale because it is usually due to chronic pulmonary disease, most commonly COPD. The “consider ischemia” read is due to slight ST depression and T-wave inversion in the anterio-lateral and inferior leads.

When the computer reads “consider ischemia,” it is important to always consider other conditions that cause ST depression and or T-wave inversion besides ACS: PE and hypokalemia are the main acute ones. Digoxin toxicity is another ones. LVH and bundle branch blocks are the main chronic ones, with WPW and MVP being less common causes. The computer printout will not put these in the differential diagnosis but you should.

This ECG is pathognomonic for hypokalemia. Only hypokalemia causes this sagging, scooped ST depression with a long QU-wave. Some call it a “wavy” pattern.

: Potassium level was 1.9 suggesting hypokalemia. The test was repeated to confirm the diagnosis. Magnesium level was normal.

The Emergency Medicine 1-Minute Consult: 

 ST depression and hypokalemia (see second image on the right).

Hypokalemia is the main cause of sagging, scooped out or wavy ST segment depression. There is often a U wave as well.

Here are links to two other interesting cases:

Prehospital Ventricular Fibrillation in a Young Woma

Massive caffeine overdose: How does the ECG fit in?

For any complaint, it is always wise to start with a broad differential diagnosis. Causes of painless acute generalized weakness and ischemic-looking EKG changes include more than just acute coronary syndrome. Consider the following:

painless PE (about 20% of PE’s are painless, usually the larger ones)

Dr. Pregerson is chief editor of http://EMresource.org, an emergency medicine website that includes a free EM ultrasound library, EM cases of the month, EM pocket references and more.

A 52-year-old female with a history of multiple sclerosis presents to the emergency department for generalized weakness and trouble swallowing. Blood tests are ordered. Can you diagnose this patient?

Case Report:  52-year-old woman with MS and generalized weakness

A 62-year-old male with history of coronary artery disease and prior coronary bypass surgery eight years ago, plus a history of anxiety and chronic obstructive pulmonary disease (COPD), presents to the emergency department after having two days of intermittent shortness of breath since starting cephalexin (Keflex) for a skin infection three days ago. He denies any chest pain, fever, new rash or cough. He states the shortness of breath seems to get worse about an hour after taking cephalexin (Keflex).

 Vital signs are normal.  Exam is otherwise normal.  Specifically, there is no rash, oral swelling, rales or wheezing.

Anxiety, allergic reaction, pulmonary embolism, acute coronary syndrome, COPD exacerbation

1. Sinus rhythm with occasional premature ventricular contractions (PVCs)
	2. Possible inferior infarct, age undetermined

The computer read is correct, but there is also some non-specific T-wave inversion and flattening in the inferior and lateral leads. The heart rate is also on the high side, but still <100.

Patient had a large mobile deep vein thrombosis in the left leg, which was asymptomatic, and multiple pulmonary embolisms in bilateral upper and lower lobes. Straightening of the interventricular septum was seen, but no massive right ventricular enlargement.


	Always be aware of medications causing symptoms but make it a diagnosis of exclusion when there are more dangerous considerations. This patient has multiple reasons he might be short of breath, but with no wheezing, an allergic reaction or COPD exacerbation are unlikely to be the cause. Even mild wheezing could be his baseline. Acute coronary syndrome and pulmonary embolism should be high on the differential diagnosis for someone with dyspnea and clear lungs.  Both are often painless. This is well known for acute coronary syndrome (ACS), but less so for pulmonary embolism, where about 20% of cases are painless.

EKG findings in pulmonary embolism are not well understood by many clinicians who think that tachycardia and S1Q3T3 (suggesting right heart strain) are the most important things to look for.  About 75% of patients with pulmonary embolism will have a normal heart rate and 60% will have a heart rate under 90. See highlighted area from sample page on the right for most common new EKG findings in pulmonary embolism and their relative incidence. These include the 4 Ts: inverted T waves, flat T waves, Tachycardia and Totally normal. Rarer findings include RBBB >R or L axis, poor R-progression (S1S2S3), among others highlighted in the image on the right.

Another important pearl in diagnosing PEs is that small PEs typically have pleuritic pain but little more. Vitals and EKG will typically all be totally normal. Large PEs are paradoxically the ones that are most likely to be painless which is likely to occur because there is no lung infarction due to collateral circulation. Large PEs, though, often painless are more likely to cause abnormal vitals and EKG findings, which often mimic those in ACS. Large PEs may also cause elevations in troponin, BNP and WBC counts, thus masquerading as ACS, congestive heart failure (CHF) or sepsis.

Your first reaction to a patient who offers you a benign cause for their symptoms should be: “I hope you’re right, but let’s make sure it’s not anything more dangerous.”

Painless pulmonary embolisms are quite common and usually occur with larger pulmonary embolisms. Painless PEs are more proximal and thus, less likely to cause lung infarction. Unlike with myocardial infarction (MI), this is just as frequent in younger patients.

Tachycardia occurs in only 25% of PEs.  If you use HR >90 it’s probably closer to 40%. This patient had a HR in the mid 90s.  A totally normal EKG is just as common. Most common are inverted or flat T-waves (about 30% each).

A 62-year-old male with history of coronary artery disease and prior coronary bypass surgery eight years ago presents to the emergency department after having two days of intermittent shortness of breath since starting cephalexin (Keflex) for a skin infection three days ago. He states the shortness of breath seems to get worse about an hour after taking cephalexin (Keflex). Can you diagnose this patient?

Author | Brady Pregerson, MD

Articles

Case Report: Asthma or Something More?

Case Report: Congestive Heart Failure?

Case Report: 52-year-old woman with MS and generalized weakness

Case Report: 62-year-old man with shortness of breath after taking antibiotic